Fernando Díaz-Basilio, Moisés Vergara-Mendoza, Jessica Romero-Rodríguez, Sharik Hernández-Rizo, Alejandro Escobedo-Calvario, Luis-León Fuentes-Romero, Santiago Pérez-Patrigeon, Akio Murakami-Ogasawara, María Gomez-Palacio, Gustavo Reyes-Terán, Wei Jiang, Joel-Armando Vázquez-Pérez, Álvaro Marín-Hernández, Dámaris-Priscila Romero-Rodríguez, María-Concepción Gutiérrez-Ruiz, Mónica Viveros-Rogel, Enrique Espinosa
Despite abundant evidence correlating T cell CD38 expression and HIV infection pathogenesis, its role as a CD4 T cell immunometabolic regulator remains unclear. We find that CD38's extracellular glycohydrolase activity restricts metabolic reprogramming after TCR-engaging stimulation in Jurkat T CD4 cells, together with functional responses, while reducing intracellular NAD and NMN concentrations. Selective elimination of CD38's ectoenzyme function licenses them to decrease the OCR/ECAR ratio upon TCR signaling and to increase cycling, proliferation, survival, and CD40L induction...
March 11, 2024: Journal of Leukocyte Biology